Damage Control Resuscitation

Chapter 7
DAMAGE CONTROL RESUSCITATION

ROB DAWES, BM, FRCA*; RHYS THOMAS, MBBS, FRCA†; and MARK WYLDBORE, MBBS, BSc (hons), FRCA‡

INTRODUCTION

THE EVOLUTION OF MILITARY TRAUMA CARE

PRINCIPLES OF DAMAGE CONTROL RESUSCITATION

Pathophysiology
Point of Wounding
Specialist Retrieval Teams
Damage Control Surgery
Permissive Hypotension
Fluids
Hemostatic Resuscitation
Point-of-Care Testing

MANAGING THE PHYSIOLOGY

Acidosis
Calcium
Potassium
Hypothermia

MEDICAL ADJUNCTS
Antifibrinolytics
Recombinant Activated Factor VII

END POINTS OF RESUSCITATION

SUMMARY

*Major, Royal Army Medical Corps; Specialist Registrar in Anaesthetics and Prehospital Care, 16 Air Assault Medical Regiment; Anaesthetics Depart-
ment, Morriston Hospital, Swansea SA6 6NO, United Kingdom
†
Lieutenant Colonel, Royal Army Medical Corps; Consultant Anaesthetist, 16 Air Assault Medical Regiment; Anaesthetics Department, Morriston
Hospital, Swansea SA6 6NO, United Kingdom
‡
Major, Royal Army Medical Corps; Anaesthetics Registrar, St. George’s Hospital, National Health Service Trust, Blackshaw Road, London SE17 0QT,
United Kingdom

85
Combat Anesthesia: The First 24 Hours
INTRODUCTION
Damage control resuscitation (DCR) is defined as
a systematic approach to major trauma, combining a
series of clinical techniques from point of wounding to
definitive treatment to minimize blood loss, maximize
tissue oxygenation, and optimize outcome. The three
major components of DCR are surgery to control bleed-
ing, massive transfusion, and hemostatic resuscitation,
instigated simultaneously (Figure 7-1).1,2
The term “damage control” originated in the United
Kingdom (UK) Royal Navy as early as the 17th centu-
ry and relates to doing whatever is required to bring
a damaged ship home to port. DCR was introduced
THE EVOLUTION OF MILITARY TRAUMA CARE
Trauma care dates back to ancient Egypt, Greece,
and Rome, inextricably linked to the wars these em-
pires were built upon. The Edwin Smith Papyrus from
the 17th century bce details the clinical treatment of 48
cases of war wounds in ancient Egypt. Homer’s Iliad
records 147 types of wound with an overall mortality
rate of 77.6% during the Trojan War. The Romans prob-
ably created the first trauma center hospitals, called
“valetudinaria,” during the 1st and 2nd centuries ce.
Eleven such centers existed in Roman Britain.7
Trauma care did not advance greatly until the 14th
century when, Guy de Chauliac (often termed the
“father of surgery”) practiced the use of inhalational
anesthesia, antisepsis, trephination, and thoracic sur-
gery. From 1797 to 1812 Dominique Larrey acted as
DAMAGE CONTROL RESUSITATION
<C>ABC
Reduced Crystalloid
Early Tourniquet
Reduced Acidosis
Specialist Retrieval
Manage Biochem
Early MT
Storm
Active Warming
Prevent
Aggressive Treatment Hypothermia
of Coagulopathy
Avoid
Vasopressors
Damage Control
Surgery
Figure 7-1. Damage control resuscitation. Surgery to control bleeding, massive transfusion, and hemostatic resuscitation are
encompassed within the the first (red) box. The positive sequelae from appropriate treatment are shown in subsequent boxes.
<C>ABC: catastrophic hemorrhage, airway, breathing, and circulation; MT: massive transfusion
86
into the UK Defence Medical Services (DMS) in 2005
with the publication of Battlefield Advanced Trauma Life
Support3 (BATLS) and later enhanced with hemostatic
resuscitation and massive transfusion guidelines.4
Further work in US military vascular trauma cases
highlighted the value of implementing this important
concept.5 DCR represents a major step in the evolu-
tion of military trauma care. Since its inception, there
has been a significant improvement in the number
of unexpected survivors and a marked reduction in
mortality from massive transfusion, despite increasing
injury severity.6
Napoleon’s surgeon general and developed what
was at the time a revolution in military trauma care:
he introduced field hospitals located close to the front
line and “flying ambulances” to quickly transport the
wounded to the operating theatre, thereby reducing
mortality in the perioperative period. Larrey under-
stood the need for predeployment training for his
ambulance teams (consisting of eight surgeons) and
exercised them daily until their operations and ap-
plication of bandages showed “the greatest degree
of emulation and that the strictest discipline were
prevalent among all the surgeons.”8
Conflict continues to drive advances in military
medicine. The sustained casualty rates since 2003
of UK military personnel in Operation Telic (Iraq)
Improved Tissue
Perfusion
Reduced Blood
Transfusion Reduced
Mortality
Effective Coagulation
Normal Electrolytes
Preservation of Tissue

and Operation Herrick (Afghanistan) have allowed
greater understanding of the pathophysiology of
major trauma and stimulated the development of new
paradigms of care and structured practice guidelines.
The new practices, which evolved into DCR, are fo-
cused on a common team approach to ensure rapid
restoration of physiology in preference to definitive
surgical treatment.1,9 To deliver effective DCR, this
approach must be rehearsed in predeployment train-
ing so that each provider becomes familiar with new
and often unfamiliar team dynamics. DCR principles
include a horizontal trauma team in which all members
(surgeons, anesthesiologists, nurses, and others) are
encouraged to contribute to the trauma management
discussion in order to solve problems and improve
care. To this end, DCR training should train those
who will be working together in future deployments.
This training has been widely termed “crew resource
management”; it aims to ensure all team members are
familiar with the environment, equipment, and roles
in future challenging DCR situations. All UK deploy-
ing clinicians attend a 5-day predeployment clinical
PRINCIPLES OF DAMAGE CONTROL RESUSCITATION
Pathophysiology
Major trauma is a generic term covering a wide
range of injuries and injury mechanisms. The physi-
cal injury itself differs according to its etiology, for
example blunt, penetrating, or blast, as well as the
individual patient. Many factors, including presence
of hemorrhage, head injury, coagulopathy, and hypo-
thermia, as well as the care given, influence the initial
physiologic insult sustained in the initial trauma.
DCR includes the accepted concepts of the “lethal
triad” of hypothermia, acidosis, and coagulopathy;
however, recent major advances in the understanding
of coagulopathy have occurred.
“Trauma-induced coagulopathy” is a term encom-
passing the coagulopathy related to the traumatic
insult and includes acidosis, hypothermia, platelet
consumption, blood loss, and dilution. More recently
a further subgroup of trauma-induced coagulopathy,
termed “acute trauma coagulopathy” (ATC), has been
described.2 This is a primary pathological event whose
cause remains uncertain, but increasing evidence points
toward a mechanism that includes tissue hypoperfu-
sion, hyperfibrinolysis, activation of protein C, and
up-regulation of thrombomodulin. The driver of ATC
appears to be related to poor tissue oxygen and results
in activation of the vascular endothelium. The endothe-
lium is a poorly understood structure that is implicated
not only in ATC but also in the development of systemic
Damage Control Resuscitation
exercise practicing challenging medical scenarios in
an exact copy of a Role 3 hospital.
During DCR it is possible that individuals, espe-
cially clinicians performing critical procedures, may
become overly focused on immediate tasks and lose
overall situation awareness (termed “reduced band-
width”). Therefore, a designated leader of the resus-
citation team must ensure effective communication
among all key members. During the initial stages of
resuscitation, the primary goal is restoring physiology,
while surgery is limited to controlling hemorrhage
and minimizing wound contamination (see Damage
Control Surgery, below). It is incumbent on the re-
suscitation leader to ensure this aim is achieved. This
may require a pause in surgery to focus on additional
dressings, packs, clamps, or direct pressure to reduce
bleeding while volume is restored by the anesthesia
team. Once volume has been restored, surgeons should
do the minimum surgery needed to save the patient’s
life. Further debridement and definitive surgery can
occur at a later stage in the evacuation process, hours
or days after the initial resuscitation.
inflammatory response syndrome, which can ultimately
lead to multiorgan dysfunction and increased mortal-
ity.10 This process occurs independently of crystalloid
administration, acidosis, and hypothermia.
DCR aims to restore tissue oxygen delivery in order
to reverse the pathological processes driven by the
hypoxic endothelium and restore normal physiology.
This approach is coupled with treatment and preven-
tion of hypothermia, acidosis, and coagulopathy. The
military approach is to target these pathologies as early
and as aggressively as is practical from the point of
wounding, along the evacuation chain, and into the
Role 3 hospital. At the Role 3 hospital, the three ma-
jor components of DCR, surgery to control bleeding,
massive transfusion, and hemostatic resuscitation, are
instigated simultaneously.1,2
Point of Wounding
Hemorrhage remains the leading cause of death
in military trauma.11 Early treatment or temporary
control at the point of wounding is essential for sur-
vival.11 Much effort has gone into improving the care
given at point of wounding.11 This includes training
in the use of the <C>ABC (catastrophic hemorrhage,
airway, breathing, and circulation) paradigm, which
is the core of the BATLS system and incorporates the
use of the hemostatic agents and the timely application
of tourniquets.
87
Combat Anesthesia: The First 24 Hours
Specialist Retrieval Teams
Care by appropriately trained prehospital doctors
(with critical care and airway skills) has been shown to
significantly improve survival from major trauma.12,13
An integral part of the British military trauma system
is the medical emergency response team (enhanced),
or MERT(E), which consists of a prehospital-trained
attending anesthesiologist or emergency physician,
two paramedics, and an emergency department flight
nurse. This specialist team is able to initiate DCR in
flight by gaining rapid intravenous or intraosseous
access and administering warm blood products with
other specific therapies such as tranexamic acid. The
ability to perform advanced airway maneuvers, di-
verting casualties to the appropriate medical facility,
and senior decision-making have contributed to the
success of this type of prehospital care. However, this
model of prehospital care is very different from what
is performed in the civilian setting or military medical
systems of other nations The MERT(E) model has been
validated since its introduction and robust evidence
of its effectiveness has been produced to guide other
services.13–15
Damage Control Surgery
Damage control surgery, the surgical component
of DCR, is focused on control of major anatomical
bleeding, removal of dead tissue, and gross decon-
tamination.16
Permissive Hypotension
Hypotensive resuscitation is a standard of practice
in hemorrhaging patients without traumatic brain
injury.17 Numerous animal models of uncontrolled
hemorrhagic shock have demonstrated improved
outcomes when a lower than normal mean arterial
pressure of 60 to 70 mm Hg is used as the target for
fluid administration during active hemorrhage.18 Two
large human trials have demonstrated the safety of
this approach (relative to the conventional target of
greater than 100 mm Hg), suggesting various benefits
including shorter duration of hemorrhage and reduced
mortality.19,20
Animal models incorporating blast injury and hem-
orrhage, however, have demonstrated a high mortal-
ity if hypotensive resuscitation is used in blast injury
patients. Follow-up studies using a prehospital blood
pressure profile (termed “novel hybrid resuscitation”)
utilized a blood pressure of 90 mm Hg (palpable radial
pulse) for 60 minutes, followed by volume boluses
to a target blood pressure of 110 mm Hg. The study
88
concluded that more animals survived overall, and for
longer, than those animals allowed 120 minutes of per-
missive hypotension. Using the results of this study’s
parameters with battlefield casualties may permit a
longer survival timeline, allowing live casualties to
reach a facility where DCR can be instigated.
Fluids
Crystalloid has been the mainstay of resuscitation
since the Vietnam War, when it was first popularized.21
In 1978 it was adapted by the American College of Sur-
geon’s Advanced Trauma Life Support Group, who ad-
vocated using two large-bore cannulas and 2,000 mL of
lactated Ringer solution for the hypotensive casualty.22
With the introduction of the DCR protocol, however,
the overall use of crystalloid has decreased dramati-
cally.23 This has helped reduce the major adverse effects
of unchecked crystalloid administration: acute lung
injury and acute abdominal compartment syndrome
(diagnosed since the Vietnam War), together with acute
renal failure, multiorgan dysfunction, and anastomotic
leaks (termed the “vicious salt water cycle”).21
Reperfusion injury is marked in hemorrhaging
trauma casualties.24 There is evidence that crystalloid
activates white cells, thereby stimulating systemic
inflammatory response syndrome. This is probably
potentiated by the “d” stereoisomer of lactate (pres-
ent in Hartmann solution), which the body fails to
metabolize.25 Over-resuscitation with crystalloid may
lead to uncontrolled hemorrhage due to dilution
of clotting factors, causing a hypocoagulable state
with the sequelae of reduced organ perfusion, and
abdominal compartment syndrome (Figure 7-2).26
These complications predispose casualties to multiple
organ failure and increased mortality, compared with
moderate resuscitation.21–26
Hemostatic Resuscitation
Hemostatic resuscitation is defined as the rapid
proactive treatment of coagulopathy associated with
major trauma27 and aims to gain physiological control
of bleeding through the use of massive hemorrhage
protocols with high ratios of packed red blood cells :
fresh frozen plasma : and platelets (PRBC:FFP:PLT),
as well as medical adjuncts guided by laboratory and
point-of-care testing. This has been shown to improve
outcomes.17 Early in resuscitation, the patient is man-
aged empirically using massive hemorrhage protocols
with the emphasis on restoring lost blood volume,
treating shock, and improving tissue oxygenation to
avoid further development of ATC. Once bleeding has
stopped and shock is reversed, a more goal-directed

Hypotension
Crystalloid Infusion
Coagulopathy SIRS MOF
Figure 7-2. Perils of over-administration of crystalloid, which
may lead to coagulopathy, systemic inflammatory response
syndrome, and multiple organ failure.
MOF: multiple organ failure
SIRS: systemic inflammatory response syndrome
approach to managing coagulopathy is advocated; its
aims are to prevent dilution, replace factors lost due
to consumption and bleeding, and treat deficiencies
caused by ATC through the administration of effec-
tive whole blood resuscitation using blood product
components (Figure 7-3). This is done with the use
of point-of-care coagulation testing such as ROTEM
(TEM International GmbH, Munich, Germany) or TEG
(Haemonetics Corp, Braintree, MA) and standard lab-
oratory blood counts. To achieve effective whole blood
replacement, PRBC:FFP:PLT ratios of approaching
1:1:1 have been advocated. Fresh whole blood is still
available to the deployed clinician.
Point-of-Care Testing
Point-of-care testing is becoming increasing im-
portant and recognized as crucial to the treatment of
the patient during DCR. It includes arterial blood gas
analysis and coagulation monitoring using thromboe-
lastometry (ROTEM or TEG). Either ROTEM or TEG
can determine failure in each part of the clotting cas-
MANAGING THE PHYSIOLOGY
The evolution of DCR philosophy, coupled with
increased training and experience in current conflicts,
has resulted in very effective and aggressive adminis-
tration of large amounts of blood products according
Damage Control Resuscitation
TRAUMA
Hemorrhage
Shock
LETHAL TRIAD
Hypothermia
Acidosis
ATC
Hypoperfusion
COAGULATION Hyperfibrinolysis
Thrombomodulin
Activated Protein C
HEMOSTASIS
Figure 7-3. Hemostatic resuscitation.
ATC: acute trauma coagulopathy
cade from clot initiation to propagation, amplification,
and stabilization. Recent clinical use of ROTEM with
experimental use of platelet function analysis (multi-
plate) has implied that platelet function is affected
early in trauma, so some new guidelines now incor-
porate the early, empiric use of platelets rather than
using the traditional trigger of a platelet count below
100.28 Point-of-care testing gives results to clinicians in
a clinically relevant time, allowing them to concentrate
on delivering blood and blood products to the patient,
and reduces the logistical delay and burden on labo-
ratories. Ultimately it allows for more individualized
patient treatment.
to massive hemorrhage protocols. Massive transfu-
sion rapidly treats underlying hemorrhagic shock
but, unless carefully monitored, has potentially lethal
sequelae. Base deficit, calcium, and potassium levels
89
Combat Anesthesia: The First 24 Hours
are all available in point-of-care blood gas analysis and
should be performed at least every 30 minutes in the
early stages of resuscitation.
Acidosis
Virtually all coagulation stages are inhibited by
acidosis. Platelets alter shape at a pH below 7.4, and
Ca2+ binding sites are pH-dependent,29 but the main
process inhibited is thrombin generation.30 Unsurpris-
ingly, trauma nonsurvivors were more likely to have a
lower pH than survivors.26 Martini et al demonstrated
that thrombin generation was inhibited by a pH of 7.1
by as much as 50% with an additional 35% reduction in
fibrinogen. Platelet count was also reduced by 50%.30
In addition to pH, base deficit is a sensitive indicator
of hypoperfusion and correlates with mortality.26 At
levels below -12.5, it has been demonstrated to directly
inhibit coagulation.30–32 Base deficit has also been used
to predict transfusion requirements.33 A recent review
concluded that a notable impairment of hemostasis
arises at a pH of 7.1 and below, with similar effects ob-
served at base deficit of -12.5 or less.34 Thus, when there
is severe hemorrhage and acidemia, buffering toward
physiologic pH values is advantageous, especially
when massive transfusions of older PRBCs displaying
exhausted red blood cell buffer systems are used.30
Calcium
JR Green was the first to show that “calcium is
instrumental in bringing about coagulation when
added to plasma which shows little or no tendency to
clot, and that coagulation in its absence is almost or
quite prevented”(1887).31 Hypocalcemia is common
in critically ill trauma patients and is associated with
increased mortality.32,33 It has since been shown that
calcium is required for several reactions in the coagu-
lation cascade and in platelet activation.32–34 Citrate (a
chelating agent) is added to blood products (FFP in
particular) to prevent clotting during storage. It follows
that a patient receiving a massive transfusion will be
hypocalcemic and coagulopathic regardless of other
measures taken to improve coagulation. It is recom-
mended that ionized calcium levels be maintained
above 1.0 mmol/L for effective coagulation to occur.35
Potassium
Hyperkalemia is common after PRBC transfusion,
and often severe.36 It appears to be more common
after transfusion under pressure and with older units
of PRBCs, most likely due to increased cell lysis. It is
therefore essential to closely monitor potassium levels
90
throughout the resuscitation and maintain a concen-
tration within the normal range. If hyperkalemia is
detected, the myocardium should be protected by ad-
ministering calcium and starting an insulin/dextrose
infusion immediately to regain control.
Hypothermia
The causes of hypothermia in the trauma patient
are reduced heat production and increased heat loss.
Hypovolemic shock results in an inadequate oxygen
delivery to the tissues, which impairs cellular respi-
ration and results in a decreased heat production.
Hypotension and hypovolemia inhibit shivering,
preventing this normal response to hypothermia.
Increased heat loss occurs through environmental
exposure and, during the resuscitation phase, is
primarily caused by administering cold fluids. Heat
loss is proportional to the volume given and the
temperature difference between the patient and the
fluid.37 The energy needed by the body to warm 2,000
mL of fluid infused at 25o C within 1 hour exceeds the
energy that can be delivered by conventional warm-
ing methods in the same time.38
Hypothermia has effects on all body systems,
including reduced cardiac output and impaired re-
spiratory and endocrine function. During DCR, its
most significant effect is on coagulation, producing a
reduction in platelet function and number, inhibition
of the coagulation cascade, and increased fibrinolytic
activity.39A significant effect on platelet function is
observed even in mild hypothermia (34 o C) through an
inhibition of thromboxane B2 and reduced expression
of surface molecules, leading to poor aggregation. At
the same temperature the reduction in platelet num-
bers is due to sequestration in the liver and spleen.40
Coagulation cascade enzyme reactions are strongly
suppressed by hypothermia. In one study, a tempera-
ture of 34o C was the critical point at which enzyme
activity in trauma patients slowed significantly. At
temperatures below 33o C, hypothermia produces a
coagulopathy equivalent to 50% of activity at nor-
mothermia, despite the presence of normal clotting
factor levels.41It is important to note that this effect on
coagulation occurs even in isolated areas of the body,
and superficial cooling of a limb with preserved core
temperature results in a significantly prolonged bleed-
ing time. It should also be noted that tests of coagula-
tion are performed at 37 oC, so a purely hypothermia-
induced coagulopathy will not be demonstrated by
laboratory tests.26
Avoiding and correcting hypothermia is critical in
preventing or correcting coagulopathy in a patient
receiving massive transfusion. The resuscitation and

operating rooms must be warmed. All fluids admin-
istered must pass through a warmer. Hot air convec-
tion should be used above the patient, and electric
mattresses under the patient have been proven useful
MEDICAL ADJUNCTS
Antifibrinolytics
The 2010 CRASH-2 trial showed that administering
tranexamic acid to adult trauma patients with, or at
risk of, significant hemorrhage within 8 hours of injury
reduced all-cause mortality with no apparent increase
in vascular occlusive events.42 As a consequence of
this trial, tranexamic acid has been incorporated into
trauma treatment protocols worldwide. A further
analysis of the CRASH-2 study demonstrated a 32% in-
creased survival if the tranexamic acid is given within
3 hours to bleeding trauma patients, but beyond this
time it is less effective and could be harmful. The trial
protocol involved administering 1 g as soon as pos-
sible, followed by another 1 g administered over the
subsequent 8 hours. This procedure rarely takes place
in military medicine because the first dose is often
administered near the point of wounding (eg, during
the MERT(E) stage), and then further blood products
and adjuncts are given when further laboratory or
thromboelastometry results are known.
Recombinant Activated Factor VII
Factor VII is a crucial component of coagulation,
binding to tissue factor (a lipoprotein present in en-
dothelial cells) exposed by injury, generating activated
factor X and subsequently thrombin. Recombinant
activated factor VII (rFVIIa) is licensed for use in
END POINTS OF RESUSCITATION
DCR is a concept aimed at restoring physiology, and
end points are critical in determining when aggressive
protocols should cease and more measured approach-
es begun. Current end points are summarized in
Figure 7-4. Critical to resuscitation is returning blood
pressure to normal values when central circulation
is filled. However, the patient still requires further
resuscitation to ensure that peripheral circulation is
also filled. To achieve this, targeted resuscitation must
continue after blood pressure returns to normal. Many
approaches to targeted resuscitation may be used, but
most military proponents now administer a high-dose
opioid anesthetic similar to cardiac anesthesia. This
procedure causes a degree of vasodilatation allowing
resuscitation of the peripheral compartment. It is fair
Damage Control Resuscitation
when multiple body cavities are being operated on
simultaneously. The patient should be insulated as
much as possible, which can be difficult when large
surgical exposure is required.
patients with hemophilia and inhibitory antibodies.
Its enhancement of hemostasis directly at the site of
injury has stimulated research into possible uses in
trauma.43,44 Two parallel, multi-center, randomized
controlled trials have shown a statistically significant
reduction in blood transfusion requirements in blunt
(but not penetrating) trauma patients treated with
rFVIIa.45 Although the trial and statistics have been
the subject of criticism, these studies remain some
of the best evidence available. The effectiveness of
rFVIIa (not limited to trauma) has also been assessed
by a Cochrane review, which concluded that rFVIIa as
a hemostatic adjunct in trauma remains unproven.46
The benefit of using rFVIIa must be balanced
against its thrombogenic potential.47 Although not
licensed for the treatment of traumatic hemorrhage,
rFVIIa use continues. Given its substantial cost, fur-
ther research is warranted. Previously, it had been
DMS policy to give rFVIIa to any salvageable patient
with continuing hemorrhage that has failed surgi-
cal and nonsurgical treatments. However, with the
advent of DCR, patients are now less coagulopathic,
acidotic, and hypothermic, and consequently the use
of rFVIIa has declined considerably. During mature
operations such as Afghanistan the use of rFVIIa is
now limited; however, in less well located and sup-
ported hospitals, there may be potential for the use
of rFVIIa to help reduce blood usage and extend
resuscitation timelines.
to say that end points of resuscitation remain uncer-
tain; however, markers of tissue perfusion are likely
to provide the most information about whole-body
tissue oxygenation.
Future strategies are focusing on the treatment of
coagulopathy with statins, with optimum ratios of FFP
: PRBC : platelets, and earlier use of blood products,
such as in the prehospital phase. Ongoing military
research involves the use of prehospital recombinant
erythropoietin and better use of blood products in the
prehospital phase by using freeze dried plasma (Ly-
oplas; DRK-Blutspendedients West gGmbH, Hagen,
Germany) and synthetic hemoglobin. Recent work
with dogs cooled to below 18°C to ascertain whether
surgery at this temperature would “suspend” further
91
Combat Anesthesia: The First 24 Hours

tissue damage and allow trauma surgery to be under- +

taken with lower risk has moved into human trials. Blood Loss Hypovolemia
Also, work has recently begun at the UPMC Presby-
terian Hospital in Pittsburgh, Pennsylvania, with deep –
hypothermia for trauma victims, termed emergency
preservation and resuscitation. Lead researcher Dr
Sam Tisherman and his team of surgeons are hoping – –
DCR
to replicate animal research in this area. Probably the
greatest advances in care will occur with earlier and –
more targeted treatment in the prehospital phase, + ACT +
particularly where long transport times are prevalent.
Prehospital systems in Europe are already trialling the
Hypothermia
use of extracorporeal membrane oxygenation, and the –
first prehospital resuscitative endovascular balloon of +
the aorta (REBOA) has already been used successfully
in London. Early use of synthetic blood products, bet- +
ter patient warming, intelligent tasking of doctor-led
prehospital teams, and shortened on-scene times, to- Coagulopathy Acidosis
gether with early computed tomography scanning, will +
allow time to surgery to be reduced in those patients
who require it. These efforts hold promise to improve
outcomes and reduce morbidity. Figure 7-4. End points of damage control resuscitation.

SUMMARY

DCR is a complex process that aims to restore physiol- rapidly restored, and surgical options increased. It is a tech-
ogy in order to save life. If practiced effectively by well-re- nique that requires flexibility, a thorough understanding of
hearsed, experienced teams, life can be saved, physiology the pitfalls of massive transfusion, and attention to detail.

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